Myocarditis and pericarditis

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Transcript Myocarditis and pericarditis

Dr .Ali. M Somily
Prof . Hanan A. Habib
Department of Pathology
Objectives
 Describe the epidemiology, risk factor for myocarditis.
 Explain the pathogenesis of myopericarditis.
 Differential between the various types of myocarditis and
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pericarditis.
Name various etiological agents causing myocarditis and
pericarditis.
Describe the clinical presentation and differential
diagnosis of myocarditis and pericarditis.
Discuss the microbiological and non microbiological
methods for diagnosis of myocarditis and pericarditis.
Explain the management ,complication and prognosis of
patient with myocarditis and/or pericarditis.
Myocarditis
 Myocarditis is inflammatory disease of the heart muscle.
 Mild & self-limited with few symptoms OR severe with
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progression to congestive heart failure & dilated cardiac
muscle.
localized or diffuse
Myocarditis can be due to a variety of infectious and non
infectious causes.
Viral infection is the most common cause
Others like toxins ,drugs and hypersensitivity immune
response.
Myocarditis
Epidemiology ,Etiology and Risk
Factors
 Epidemiology : no accurate estimate of incidence as
many cases are mild & brief and diagnosis is not made.
 Coxsackie virus B is the most common cause of
myocarditis
 Other virus like Coxsackie virus A, Echoviruses,
Adenoviruses ,Influenza, EBV, Rubella, Varicella,
Mumps, Rabies, Hepatitis viruses and HIV.
 Bacterial causes include Corynebacterium
diphtheriae, Syphilis ,Lyme disease or as a
complication of bacterial endocarditis.
 Parasitic cause includes Chagas diseases, Trichinella
spiralis, Taxoplasma gondii and Echinococcus.
 Others organisms includes Rickettsiae, Fungi,
Chlamydia, enteric pathogens, Legionella and
Mycobacterium tuberculosis.
 Giant cell myocarditis due to Thymoma, SLE
(Systemic Lupus Erythematosus ) or Thyrotoxicosis.
Infectious
Noninfectious
Viruses
1. Coxsackie B
2. HIV
Systemic Diseases
1. SLE
2. Sarcoidosis
3. Vasculities(Wegener’s
disease)
4. Celiac disease
Bacterial
1. Corynebacterium diphtheriae
(diphtheria)
Neoplastic infiltration
Protozoan
1. Trypanosoma cruzi (Chagas
disease)
Drugs & Toxins
1. Ethanol
2. Cocaine
3. Radiation
4. Chemotherapeutic agents Doxorubicin
Spirochete
Clinical Presentation
 Highly variable ; days to weeks after onset of acute
febrile illness or with heart failure without any known
antecedent symptoms .
 Fever, headache, muscle aches, diarrhea, sore
throat and rashes similar to any viral infection
 Chest pain, arrhythmias ,sweating , fatigue and may
present with congestive heart failure.
Differential Diagnosis
 Acute Myocarditis
 Vasculitis
 Cardiomyopathy ( due to drugs or radiation)
Diagnosis
 WBCs, ESR, Troponine and CK-MB usually elevated
 ECG (nonspecific ST-T changes and conduction delays are common)
 Blood cultures
 Viral serology and other specific test for Lyme
disease, diphtheria and Chagas disease may be
indicated on a case by case basis.
 Chest X-rays : show cardiomegaly
 Radiology : MRI and Echocardiogram
 Heart muscle biopsy
ECG of normal heart
Endomyocardial Diagnosis
 Pathologic exam may reveal lymphocytic
inflammatory response with necrosis, but this is not
sensitive because of the patchy areas of distribution.
 “Dallas” criteria for histopathologic diagnosis
 “Giant cells” may be seen.
Giant cells-myocarditis
Management
 Often supportive;
 Restricted physical activity in heart failure.
 Specific antimicrobial therapy is indicated when an
infecting agent is identified.
 Treatment of heart failure arrhythmia
 Other drugs indicated in special situations like
anticoagulant, NSAID (nonsteroidal antiinflammatory drugs) ,
steroid or immunosuppressive immunomodulatory
agents.
 Heart transplant
Management
 Most cases of viral myocarditis are self limited.
 One third of the patients are left with lifelong
complications, ranging from mild conduction defects
to severe heart failure.
 Patient should be followed regularly every 1-3 months.
 Sudden death may be the presentation of
myocarditis in about 10% of cases.
Pericarditis
 Pericarditis is an inflammation of the pericardium
usually of infectious etiology ( viruses, bacterial,
fungal or parasitic)
Viral Pericarditis:
 Coxsackievirus A and B, Echovirus are the most
common causes.
 Other viruses includes Herpes viruses, Hepatitis B ,
Mumps, Influenza, Adenovirus ,Varicella and HIV.
Pathophysiology
 Contiguous spread
 lungs, pleura, mediastinal lymph nodes, myocardium,
aorta, esophagus, liver.
 Hematogenous spread
 septicemia, toxins, neoplasm, metabolic
 Lymphangetic spread
 Traumatic or irradiation
Pathophysiology
 Inflammation provokes a fibrinous exudate with or
without serous effusion
 The normal transparent and glistening pericardium is
turned into a dull, opaque, and “sandy” sac
 Can cause pericardial scarring with adhesions and
fibrosis.
 Bacterial Pericarditis usually a complication of
pulmonary infections (e.g. pneumonia ,empyema):
S. pneumonia, M. tuberculosis, S. aureus, H. influenzae,
K. pneumoniae & Legionella.
 HIV patients may develop pericardial effusions
(M.tuberculosis , M. avium complex).
 Disseminated fungal infection (Histoplasma,
Coccidioides)
 Parasitic infections (disseminated toxoplasmosis,
contagious spread of Entamoeba histolytica )are rare
causes.
Types of Pericarditis
 Caseous Pericarditis commonly tuberculous in
origin.
 Serous Pericarditis due to autoimmune diseases
(rheumatoid arthritis, SLE).
 Fibrous Pericarditis a chronic pericarditis usually
suppurative, caseous, or encased in a thick layer of scar
tissue.
Types of Effusive Fluid
 Serous
 Transudative - heart failure
 Suppurative
 Pyogenic infection with cellular debris and large
number of leukocytes
 Hemorrhagic
 Occurs with any type of pericarditis especially with
infections and malignancies
 Serosanguinous
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Constrictive Pericarditis
 Idiopathic
 Radiotherapy
 Cardiac surgery
 Connective tissue disorders
 Dialysis
 Bacterial infection
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Clinical presentation
 Patients with pericarditis will present with sudden
pleuretic chest pain, fever, dyspnea and a friction rub.
 Patient with tuberculous pericarditis has insidious
onset of symptoms.
 On examination exaggerated pulses , paradoxus JVP
and tachycardia.
 As the pericardial pressure increases, palpitations ,
presyncope or syncope may occur.
Tuberculous Pericarditis
 Incidence of pericarditis in patients with pulmonary
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TB ranges from 1 – 8 %
Physical findings: fever, pericardial friction rub,
hepatomegaly
Tuberculin skin test usually positive
Fluid smear for AFB often negative
Pericardial biopsy more definitive
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Acute Pericarditis
Differential Diagnosis
 Acute myocardial infarction
 Pulmonary embolism
 Pneumonia
 Aortic dissection
Diagnosis
 ECG will show ST elevation, PR depression and T-wave
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inversion may occur later.
Blood culture
Leukocytosis and an elevated ESR are typical
Other routine testing : urea and creatinine.
Tuberculin skin test is usually positive in tuberculous
pericarditis.
Chest x-ray may show enlarged cardiac shadow or calcified
pericardium and CT scan show pericardial thickening
>5mm.
Pericardial fluid or pericardial biopsy specimens for fungi,
antinuclear antibody tests and Histoplasmosis complement
fixation indicated in endemic area.
Management
 Management is largely supportive for cases of
idiopathic and viral pericarditis including bed rest ,
NSAIDS ( non-steroidal anti-inflammatory drugs) and
Colchicine.
 Corticosteroid is controversial and anticoagulants
usually contraindicated.
 Specific antibiotics must include activity against S.
aureus and respiratory bacteria.
 Antiviral:
Acyclovir for Herpes simplex or Varicella . Ganciclovir
for CMV .
Management
 Pericardiocentesis to relief tamponade.
 Patients who recovered should be observed for
recurrence.
 Symptoms due to viral pericarditis usually subsided
within one month.
Pericardiocentesis